Faculty Collaboration Database

Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism. Am J Physiol Heart Circ Physiol 2001 Nov;281(5):H2097-104

Date

10/23/2001

Pubmed ID

11668071

DOI

10.1152/ajpheart.2001.281.5.H2097

Scopus ID

2-s2.0-0035200038 (requires institutional sign-in at Scopus site)   82 Citations

Abstract

We tested the hypothesis that hyperglycemia alters retrograde coronary collateral blood flow by a nitric oxide-mediated mechanism in a canine Ameriod constrictor model of enhanced collateral development. Administration of 15% dextrose to increase blood glucose concentration to 400 or 600 mg/dl decreased retrograde blood flow through the left anterior descending coronary artery to 78 +/- 9 and 82 +/- 8% of baseline values, respectively. In contrast, saline or L-arginine (400 mg x kg(-1) x h(-1)) had no effect on retrograde flow. Coronary hypoperfusion and 1 h of reperfusion decreased retrograde blood flow similarly in saline- or L-arginine-treated dogs (76 +/- 11 and 89 +/- 4% of baseline, respectively), but these decreases were more pronounced in hyperglycemic dogs (47 +/- 10%). L-arginine prevented decreases in retrograde coronary collateral blood flow during hyperglycemia (100 +/- 5 and 95 +/- 6% of baseline at blood glucose concentrations of 400 and 600 mg/dl, respectively) and after coronary hypoperfusion and reperfusion (84 +/- 14%). The results suggest that hyperglycemia decreases retrograde coronary collateral blood flow by adversely affecting nitric oxide availability.

Author List

Kersten JR, Toller WG, Tessmer JP, Pagel PS, Warltier DC

MESH terms used to index this publication - Major topics in bold

Animals
Arginine
Collateral Circulation
Coronary Circulation
Disease Models, Animal
Dogs
Hyperglycemia
Microcirculation
Myocardial Ischemia
Myocardial Reperfusion Injury
Nitric Oxide